SUPPRESSION AND RESTORATION OF V-SRC EXPRESSION IN RSV TRANSFORMED-CELLS AFTER TRANSFECTION WITH N-RAS AND ITS ANTAGONIST

Previously, it was shown that hamster cells transformed by Rous Sarcom a Virus (RSV) exhibited a decreased expression of the RSV products (in cluding the pp60 src oncogene) when these cells were supertransfected with the N-ras oncogene. To assess the responsibility of the activated N-ras in the modulation of the RSV viral products, a strategy based o n two ras antagonists was used; i.e. i) a rap1A/K-rev1 expression vect or known for its capacity to revert the K-ras induced transformed phen otype and ii) a plasmid containing antisense N-ras sequence. We presen t data showing only the plasmid construct containing the N-ras antisen se sequense could inhibit expression or N-ras and, at the same time, r estore the expression of v-src, up to a level comparable to that of th e parental cells. Our results support the idea that some biological sw itches, triggered and activated through the N-ras oncogene pathway, mi ght modulate the promoter activity of the RSV LTR.